Cicatricial alopecia

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Meet the patient

A 64-year-old postmenopausal woman has watched her frontal hairline creep backwards for eighteen months. The skin it used to sit on is now smooth, pale and shiny, with no holes where hairs should be. A single terminal hair stands alone at the advancing edge — the last soldier of a retreating army. Her eyebrows are thinning too.[1][6]

Two questions settle her next year, and they settle every cicatricial alopecia: are the follicular ostia gone? (the dermatoscope answers in ten seconds) and is the margin still inflamed? (the answer decides whether anything can still be saved). Hold those two questions and the whole topic falls into place.[1]

Lost ostia are lost forever — the definition

Cicatricial alopecia is not one disease, it is one final common pathway: a follicle killed and replaced by scar. The word is honest about the outcome — cicatricial comes from the Latin cicatrix, a scar. Wherever the follicle's stem-cell home is destroyed, collagen moves in, and the skin remembers nothing of the hair that used to be there.[2][5]

The single clinical sign that separates scarring from non-scarring alopecia is the absence of follicular ostia — the tiny surface openings disappear. In androgenetic alopecia, alopecia areata or telogen effluvium the follicle survives, so regrowth stays possible. In cicatricial disease the opening is gone, and gone is permanent.[2]

Split the cause into primary (inflammation targets the follicle itself) versus secondary (an outside force — burn, radiation, kerion, tumour — flattens an innocent follicle). Primary disease is uncommon, with prevalence quoted between 0.02 and 0.11 percent, but the cosmetic blow is permanent, so the quality-of-life toll runs high.[5][8]

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The NAHRS split — classify by the infiltrate, then treat it

The classification is not academic — it is your prescription pad. The NAHRS consensus sorts primary disease by what the biopsy shows, and each group answers to a different drug family.[2][6]

Lymphocytic group — the immune-attack family

A band-like or perifollicular lymphocytic infiltrate attacks the upper, permanent follicle — the isthmus and bulge where the stem cells live. Five names to carry into the viva:[1]

• Lichen planopilaris (LPP) — the prototype lymphocytic cicatricial alopecia.
• Frontal fibrosing alopecia (FFA) — the frontal-temporal variant of LPP, classic in postmenopausal women.
• Discoid lupus erythematosus (DLE) — chronic cutaneous lupus landed on the scalp.
• Central centrifugal cicatricial alopecia (CCCA) — the commonest scarring alopecia in women of African ancestry.
• Pseudopelade of Brocq — the burnt-out end-stage, "footprints in the snow", usually the ashes of old LPP or DLE.

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Neutrophilic group — the pus-and-sinus family

Neutrophils pile into and around the follicle, and you see pustules, abscesses and sinus tracts. Two diseases dominate:[1]

• Folliculitis decalvans — recurrent pustules and tufted hairs, with Staphylococcus aureus usually on the swab.
• Dissecting cellulitis of the scalp (perifolliculitis capitis abscedens et suffodiens — literally "abscessing and burrowing") — deep, boggy, interconnecting nodules and sinuses.

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Mixed group

A mixed infiltrate appears in:[1]

• Acne keloidalis nuchae (AKN) — fibrosing folliculitis of the nape, almost confined to Black men.
• Acne necrotica — superficial pustules healing with varioliform scars.
• Erosive pustular dermatosis of the scalp — a pustular, eroding process on traumatised, sun-damaged scalp.

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Secondary cicatricial alopecia

NAHRS leaves secondary disease out of its scheme because the follicle dies from the outside, not from a primary folliculocentric attack. Think burns, ionising radiation, severe infection (kerion, cutaneous TB, tertiary syphilis), infiltrating scalp malignancy, and surgical or chronic-traumatic injury. In low-resource settings, tinea kerion and destructive pyogenic infection are still the preventable causes of childhood scarring alopecia — and the ones the exam loves.[3][6]

Who gets it — the demographic fingerprint

Each subtype carries a patient on its back. Learn the patient and you name the disease before you sit down.[1]

LPP favours women about three to one and lands on Caucasian women in their forties to sixties. FFA is overwhelmingly postmenopausal, onset 50 to 70 years — though premenopausal women and men now turn up in every series. CCCA is the commonest scarring alopecia in women of African ancestry, beginning in the thirties to fifties and crawling outward from the vertex over years; tight braids, weaves, locs, chemical relaxers and heat all feed it, and the name central centrifugal literally describes where it starts and how it moves.[1][6]

Folliculitis decalvans takes men more than women, in early-to-mid adulthood, often with chronic nasal S. aureus carriage. Dissecting cellulitis is a disease of young Black men and is one limb of the follicular occlusion tetrad — with acne conglobata, hidradenitis suppurativa and pilonidal sinus. AKN is nearly confined to Black men and tracks close shaving of curly nape hair plus collar and helmet friction.[9]

A newer thread the fellowship examiner now probes: lymphocytic subtypes travel with metabolic comorbidity — dyslipidaemia, diabetes, hypertension, and probably cardiovascular disease — through shared inflammation, obesity-driven hormonal change, and the inactivity that hair-loss distress breeds. In DLE, ultraviolet light and smoking are the environmental triggers that drive activity and scarring.[3][7][5][8]

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The stem-cell niche dies first — why the loss is permanent

Everything irreversible in this topic comes down to one structure: the follicular stem-cell niche. The permanent upper follicle — the isthmus and bulge — holds the epithelial stem cells that rebuild the lower follicle every cycle. Destroy the bulge and the follicle cannot repopulate; collagen fills the empty tract and the surface opening vanishes.[5][8]

In lymphocytic disease, autoreactive or aberrantly activated T cells swarm the infundibulum and isthmus. The sebaceous gland is an early casualty — its loss is a near-universal histology finding. Interferon-γ, TNF-α and interleukin-17 drive a lichenoid interface reaction, while TGF-β switches on fibroblasts and lays down collagen. Epithelial cells may even undergo epithelial-mesenchymal transition (EMT) — shedding their epithelial identity and turning fibroblast-like, actively building the scar.[5][8]

The unifying theory: follicular immune-privilege collapse

The anagen bulb normally hides from immunity — it dials down MHC class I and secretes immunosuppressive molecules, a state called follicular immune privilege. In alopecia areata that privilege cracks but the follicle survives. In cicatricial alopecia the attack is destructive and the stem-cell niche itself — the privileged tissue — is permanently lost, which is why scar, not regrowth, follows. This is the conceptual answer to the viva question "why does alopecia areata regrow but cicatricial alopecia does not?"

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In neutrophilic disease the neutrophils answer bacterial colonisation or a primary follicular-occlusion defect. The inflammation punches through the follicular wall, lets neighbouring follicles merge into the tufted hairs of folliculitis decalvans, and throws up abscesses, sinuses and granulation. In AKN, chronic inflammation tips the keloid-prone scalp into hypertrophic scarring.[3][7]

The active margin — treat the border, not the scar

One idea organises the whole clinical exam: a cicatricial patch has two zones, and only one of them is still alive. The patient's first complaint is often not hair loss at all but itch, burn, pain or tenderness (trichodynia) at the inflamed edge. In darker skin, post-inflammatory pigment change rings the margin and may dominate the picture.[1]

The shared physical signs:[1]

• A bald patch with an irregular or smooth border.
• Loss of follicular ostia in the bald skin — smooth, shiny, atrophic.
• Erythema and scale at the active inflammatory margin.
• Perifollicular hyperkeratosis — white scaly collarettes around surviving hairs, the LPP/FFA fingerprint.
• Tufted hairs — many shafts from one dilated opening, pathognomonic for folliculitis decalvans.
• Pustules, crusting, nodules, sinuses or keloid in neutrophilic or mixed disease.

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The active inflammatory margin is where the disease — and your treatment — lives. The border is red, scaly, pustular or indurated; the centre is pale, smooth and devoid of openings. You treat the border. The centre is already a grave.[1]

The atypical presentations are the ones examiners reach for. FFA can take the eyebrows, eyelashes and body hair, and may sit with facial papules. CCCA may announce itself with mild scaling or burning before hair loss is visible. Pseudopelade shows "footprints in the snow" — small white atrophic patches with no active inflammation at all. Dissecting cellulitis impersonates infection with its boggy abscesses. And in a child, scarring alopecia is rare enough that you must first exclude tinea capitis (especially kerion), trichotillomania with chronic traction, and inflammatory skin disease.[2][4][6]

The first fork — scarring versus non-scarring

Before you classify scarring alopecia, prove it is scarring. Non-scarring alopecia is far commoner, and once you have wrongly labelled a patient cicatricial you have written off regrowth that was always possible.[1]

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The face-off beneath the table: alopecia areata gives smooth patchy loss with preserved ostia and exclamation-mark hairs at the edge; androgenetic alopecia preserves the frontal hairline in women and shows miniaturised hairs; cicatricial disease does neither — the ostia are gone.[1]

Traction alopecia is the great chameleon. Early, it is reversible and the ostia survive; late, after years of tight braids or weaves, it scars and the openings vanish — the same patient crosses the line from non-scarring to scarring. Tinea capitis scales, breaks hairs and gives occipital lymphadenopathy; a kerion left untreated scars. Trichotillomania leaves bizarre patches of varied-length hairs on a non-scarred scalp. Wood's lamp, KOH microscopy and fungal culture settle the infectious mimics.[1]

Never forget the secondary causes when the history fits: a burn, radiotherapy, scalp surgery, severe infection, or a slowly enlarging plaque that may be squamous cell carcinoma, basal cell carcinoma or lymphoma. In long-standing DLE or dissecting cellulitis, a non-healing ulcer is Marjolin squamous cell carcinoma until biopsy proves otherwise.[2][4][6]

The bedside round — dermatoscope first, biopsy the margin

Your dermatoscope answers the scarring question in ten seconds; your biopsy answers the subtype question only if you site it correctly. Map the pattern, confirm whether openings are present, find the active inflammation, and hunt for pustules, crusting, scale, keloid and sinuses.[1]

Run the focused examination in this order:[1]

1. Inspect the whole scalp — pattern (vertex, frontal, patchy, diffuse), symmetry, scarring.
2. Palpate — scar is smooth, shiny, firm; active inflammation is indurated, boggy or tender.
3. Check the follicular ostia under the dermatoscope — the single most important discriminator.
4. Hair-pull test — grasp about 50 hairs and pull gently; over 5 to 6 hairs suggests active shedding, but a burnt-out scar is pull-negative because there is nothing left to extract.
5. Trichoscopy to pattern-match (below).
6. Biopsy the active inflammatory margin — a 4 mm punch at the junction of normal and scarred skin, not the centre.
7. Photograph — serial standardised photos are how you judge response over months.

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Four named bedside signs earn marks every time:[1][2][4]

• Lonely hair sign — a single terminal hair at the advancing frontal hairline in FFA; the last follicle standing.
• Carpet-tack sign — lift the adherent scale of DLE and follicular plugs stud its underside, like a carpet tack.
• Tufted hairs — many shafts from one ostium in folliculitis decalvans; "doll's hair" or "paintbrush" hair.
• Footprints in the snow — small white atrophic patches of burnt-out pseudopelade.

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Investigations — trichoscopy, then a correctly sited biopsy

Two investigations do almost all the work: the dermatoscope at the bedside and a 4 mm punch from the active margin.[1]

Trichoscopy

The universal hallmark is loss of follicular openings. Layer on the subtype signatures:[1]

• Lymphocytic disease — perifollicular scale, perifollicular erythema, white dots (scarred openings), tubular hair casts, and patches of total ostial loss.
• FFA — lonely hair sign, perifollicular erythema and scale at the frontal margin, ostial loss across the frontal band.
• DLE — thick arborizing vessels, white structureless areas, keratotic plugs, prominent scale.
• CCCA — reduced vertex density, peripilar white halos, broken hairs, central ostial loss.
• Folliculitis decalvans — tufted hairs, pustules, yellowish follicular openings, haemorrhagic crusts, reduced density.
• Dissecting cellulitis — yellow structureless areas, vessels, empty follicles with minimal scale.

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Scalp biopsy

The classic trap: biopsying the centre of the scar. The centre is end-stage fibrosis and tells you nothing. Take a 4 mm punch from the active inflammatory margin — the junction of normal hair-bearing and scarred skin — deep enough to include subcutaneous fat, oriented along hair growth, and handled gently to avoid crush artefact.[1]

Histology by group:[1]

• Lymphocytic — lichenoid or perifollicular infiltrate at the isthmus, loss of sebaceous glands, follicles replaced by fibrous tract remnants; DIF shows cytoid bodies at the dermo-epidermal junction in LPP, and a lupus band (linear IgG, IgM, C3) at the basement membrane in DLE.
• Neutrophilic — intra- and perifollicular neutrophils, pustules, abscesses, granulation, later fibrous tracts; in folliculitis decalvans the merging of adjacent follicles makes the tuft.
• End-stage / burnt-out — dense fibrous tracts, absent sebaceous glands, minimal inflammation; the original subtype may be unknowable.

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Microbiology

Swab pustular or crusted lesions for Staphylococcus aureus; in neutrophilic disease the culture steers the antibiotic. If tinea is in play, send skin scrapings and hairs for KOH microscopy and fungal culture or PCR. Chronic sinuses deserve anaerobic culture.[1]

Autoimmune and systemic screening

For any DLE or lupus suspicion:[1]

• ANA by immunofluorescence.
• Anti-dsDNA, anti-Smith, anti-Ro/La, complement C3/C4 if systemic features appear.
• Full blood count, renal function, urinalysis to screen for systemic lupus.

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In the other subtypes, add thyroid function, fasting lipids, glucose or HbA1c, and iron studies — metabolic comorbidity is common and colours both counselling and management.[1]

Imaging and photography

Serial clinical photographs are the cheapest and most useful monitoring tool you own. High-frequency ultrasound and reflectance confocal microscopy stay in research. In dissecting cellulitis with extensive sinuses, CT or MRI may map disease before surgery.[4][6]

First contact — stop the inflammation before more follicles die

Cicatricial alopecia is not a cardiac arrest, but every day of active inflammation is a day of permanent follicular death. The first visit is time-critical in that narrow, important sense.[1]

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The counselling line that prevents lawsuits and broken trust: destroyed follicles cannot regrow hair. Early treatment halts progression; it never reverses established scar. Say it out loud, say it kindly, and say it early.[3][6]

Definitive therapy — the NAHRS group is your drug chart

Treatment is keyed to the inflammatory group, and the goal is to stop inflammation and preserve what remains — not to regrow what is gone. Think of it as a long, stepwise campaign, not a course of tablets.[1]

Lymphocytic disease — steroids and hydroxychloroquine

First-line — topical and intralesical corticosteroids:[1]

• Potent topical corticosteroids such as clobetasol propionate 0.05% foam, solution or shampoo to the active margin once or twice daily for 4 to 8 weeks, then taper; pulse the therapy to spare the skin from atrophy.
• Intralesional triamcinolone acetonide 2.5 to 10 mg per mL into the active margin every 4 to 6 weeks; drop to 2.5 mg per mL on the face and eyebrows to avoid atrophy. Ideal for localised LPP and FFA.

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First-line systemic — hydroxychloroquine:[1]

• Hydroxychloroquine 200 to 400 mg orally daily is the workhorse for LPP, FFA and DLE. Dose by real body weight — keep it under 5 mg per kg per day to protect the retina. Onset is slow; judge response at 3 to 6 months. Baseline and annual ophthalmology is mandatory.

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Adjunctive and second-line options:[1]

• Tetracyclines — doxycycline 100 mg twice daily or minocycline 100 mg daily; anti-inflammatory and anti-matrix-metalloproteinase, used as steroid-sparers.
• Mycophenolate mofetil 1 to 2 g daily for refractory or extensive disease; watch blood count and liver function.
• Systemic corticosteroids — prednisolone 0.5 to 1 mg per kg per day for short control of a flare, then taper onto a steroid-sparer.
• Pioglitazone 15 to 30 mg daily, a PPAR-γ agonist, as an adjunct in LPP with variable evidence.
• JAK inhibitors — tofacitinib, baricitinib, ritlecitinib — emerging off-label for refractory disease; screen for infection, watch lipids, counsel on thromboembolic and malignancy risk.
• 5-alpha-reductase inhibitors — finasteride 1 to 5 mg daily or dutasteride 0.5 mg daily, especially when FFA overlaps androgenetic alopecia.

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Neutrophilic disease — rifampicin-clindamycin and isotretinoin

Folliculitis decalvans — antistaphylococcal therapy is the cornerstone:[1]

• The classic combination is oral rifampicin 300 mg twice daily plus clindamycin 300 mg twice daily for 10 to 12 weeks — rifampicin penetrates biofilms, clindamycin silences staphylococcal toxins and inflammation, and pairing them slows resistance.
• Maintenance with doxycycline 100 mg twice daily or erythromycin or clarithromycin, because relapse is the rule.
• Antiseptic shampoos (chlorhexidine, zinc pyrithione, ketoconazole) cut colonisation; topical clindamycin and nasal mupirocin decolonise the S. aureus reservoir.
• Refractory disease: oral isotretinoin 0.5 to 1 mg per kg per day, dapsone, or a TNF inhibitor (adalimumab, infliximab).

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Dissecting cellulitis — isotretinoin is the mainstay:[3]

• Oral isotretinoin 0.5 to 1 mg per kg per day for 4 to 6 months aims at remission by shrinking sebum, normalising follicular keratinisation and damping inflammation. It is fiercely teratogenic — pregnancy prevention is non-negotiable.
• Antibiotics (doxycycline, clindamycin, trimethoprim-sulfamethoxazole) for their anti-inflammatory effect and for secondary infection.
• TNF inhibitors (adalimumab, infliximab) for refractory disease.
• Intralesional corticosteroids and surgical drainage or excision for large abscesses and sinuses — and only in quiet disease, because active disease flares after manipulation.

[3] [7]

Mixed group — acne keloidalis nuchae

AKN management follows the same logic of trigger-control then anti-inflammation:[1]

• Trigger avoidance — stop close clipping, use a grade-2 (6 mm) guard or longer, reduce collar and helmet friction.
• Topicals — clindamycin or benzoyl peroxide for pustules; topical corticosteroid or retinoid for papules.
• Intralesional triamcinolone 10 to 40 mg per mL for fibrotic plaques and keloid.
• Systemic — doxycycline, rifampicin-clindamycin, or isotretinoin for extensive disease.
• Surgery — excision of large keloidal plaques or laser epilation for persistent disease.

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Adjunctive and supportive care

• Topical minoxidil 5% does not reverse scar but can thicken surviving terminal hairs — a common adjunct in CCCA and FFA.
• Camouflage — wigs, hairpieces, scalp micropigmentation and careful styling carry enormous psychosocial weight.
• Platelet-rich plasma and low-level laser are weak-evidence adjuncts; they never replace anti-inflammatory therapy.
• Psychosocial support — hair is identity in many cultures; screen for anxiety and depression and refer when it is present.

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Hair transplantation has exactly one place — stable, burnt-out, quiescent disease. Grafting into actively inflamed scalp fails: the grafts die and the disease flares. Wait until the margin has been silent for many months before anyone reaches for a punch.[10]

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The subtypes up close — five patients to recognise on sight

Lichen planopilaris (LPP)

Patchy scarring, usually vertex or crown, with perifollicular erythema and perifollicular hyperkeratosis at the active margin and itch or burn as the complaint. Histology gives a lichenoid infiltrate at the isthmus, lost sebaceous glands, fibrous tract remnants. Treat with topical and intralesional corticosteroids plus hydroxychloroquine; escalate to mycophenolate, systemic steroid or pioglitazone.[1]

Frontal fibrosing alopecia (FFA)

Progressive frontal and temporal hairline recession in a postmenopausal woman, with the lonely hair sign at the advancing edge and eyebrow, eyelash or body-hair loss and facial papules in many. A clinical variant of LPP. Reach for 5-alpha-reductase inhibitors (finasteride, dutasteride), hydroxychloroquine, topical and intralesional corticosteroids, and mycophenolate or JAK inhibitors when needed. Strict sun protection — photo-exposure drives the hairline.[1]

Discoid lupus erythematosus (DLE)

Well-demarcated erythematous plaques with adherent scale, follicular plugging, dyspigmentation and scarring. The carpet-tack sign — follicular plugs on the underside of lifted scale — is viva gold. Five to 25 percent of DLE patients develop systemic lupus, so screen. First-line is potent topical or intralesional corticosteroids plus hydroxychloroquine; refractory disease may need thalidomide, methotrexate, mycophenolate or retinoids. Photoprotection and smoking cessation are mandatory.[3]

Central centrifugal cicatricial alopecia (CCCA)

Vertex or crown onset, centrifugal spread, women of African ancestry, fuelled by traction, relaxers and heat. The active margin shows perifollicular hyperkeratosis; the centre is scarred. Treatment is built on stopping every traumatic grooming practice, plus topical corticosteroids, intralesional triamcinolone and hydroxychloroquine, with minoxidil to prop up surviving hair. Early diagnosis matters — the central vertex is cosmetically and psychologically load-bearing.[9]

Pseudopelade of Brocq

The end-stage: small, white, atrophic patches — "footprints in the snow" — with no active inflammation. Pseudopelade is French for "false pelade", Brocq's name for a bald patch: it is not its own disease but the cold ash of old LPP or DLE. No inflammation means no immunosuppression — search for an active underlying process producing new lesions; if there is none, management is camouflage and monitoring.[1]

Folliculitis decalvans

Recurrent pustules, crusting and tufted hairs, with S. aureus usually cultured. The rifampicin-clindamycin combination for 10 to 12 weeks is standard, with maintenance antibiotics and decolonisation. Chronic relapse may need isotretinoin, dapsone or a TNF inhibitor. Nasal mupirocin and antiseptic washes cut carriage and relapse.[1]

Dissecting cellulitis of the scalp

Deep, boggy, tender nodules and abscesses communicating through sinuses — part of the follicular occlusion tetrad, and it hunts young Black men. Isotretinoin is the mainstay; refractory disease answers to TNF inhibitors; surgery waits for quiescent, localised disease. Chronic sinuses carry a real risk of squamous cell carcinoma, so biopsy any non-healing area.[7]

Acne keloidalis nuchae (AKN)

The nape of the neck in Black men: perifollicular papules and pustules ripening into keloidal plaques, tufted hairs and sinuses. A mixed cicatricial alopecia. Stop the close shaving, add topical antibiotics or retinoids and intralesional corticosteroids, escalate to systemic agents, and reserve surgery or laser epilation for refractory plaques.[1]

Complications and the pitfalls that cost marks

The complication that defines the topic is the one you cannot undo: permanent hair loss. Even perfect treatment cannot regrow scar. Around it cluster the rest:[1]

• Psychosocial morbidity — anxiety, depression, isolation; the toll is routinely underestimated.
• Secondary infection — pustules and sinuses chronically colonised with S. aureus.
• Keloid formation — especially AKN and dissecting cellulitis, and in keloid-prone skin.
• Squamous cell carcinoma — long-standing DLE and dissecting cellulitis can turn; biopsy any non-healing ulcer or nodule (Marjolin).
• Iatrogenic atrophy — prolonged potent topical or repeated high-concentration intralesional steroid thins skin, telangiectasia and striae.
• Ocular involvement — DLE on lids and conjunctiva; FFA taking the lashes.

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The pitfalls are the ones the viva is built on:[1]

• Biopsying the centre of the scar — it shows only end-stage fibrosis and gives no diagnosis.
• Treating burnt-out scar with minoxidil alone and expecting regrowth — minoxidil cannot resurrect a destroyed follicle.
• Missing tinea capitis in a child and immunosuppressing instead of giving an oral antifungal.
• Forgetting to screen for systemic lupus in scalp DLE.
• Delaying treatment while the biopsy is in the post — every day destroys more follicles.
• Hair transplanting during active disease — the grafts die and the disease flares.

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Prognosis — how early you start decides how much survives

Prognosis tracks one variable: how quickly inflammation is brought under control. Established scar is permanent, but progression can almost always be halted with prompt, well-chosen treatment. The realistic endpoint is stabilisation and preservation, not restoration.[1]

Favourable signs: early diagnosis with limited involvement, a brisk response to first-line therapy (fading erythema, scale and pustules, halted expansion), good adherence and trigger avoidance, and no keloid tendency. Poor signs: late presentation with extensive central scar, rapid progression despite first-line therapy, keloid or extensive sinus disease, ongoing traction, chemical processing or smoking, and non-adherence.[1]

Most patients live in the outpatient clinic. Interval follows activity: monthly intralesional injections for active LPP or FFA, every 6 to 12 weeks for stable patients on hydroxychloroquine, and urgent review for new pustules, nodules, rapid expansion or a non-healing ulcer. Teach patients to photograph their scalp between visits — progression is slow and the eye forgets.[1]

Special populations

Pregnancy and breastfeeding

Rewrite the prescription pad for pregnancy. Avoid isotretinoin, finasteride, dutasteride, methotrexate, mycophenolate, thalidomide and TNF inhibitors. Hydroxychloroquine is generally safe and is continued in lupus pregnancy because the flare risk outweighs the drug risk. Use topical and intralesional corticosteroids cautiously — limit amount and avoid potent agents over large areas. Stop tetracyclines after the first trimester (fetal bone and teeth). Rifampicin is best avoided unless essential. Breastfeeding mirrors these cautions; decide case by case.[1]

Children

Scarring alopecia is uncommon in children, and the commonest cause is tinea capitis — especially kerion — which needs oral antifungal (griseofulvin or terbinafine), not immunosuppression. Trichotillomania and traction are common but usually reversible. Juvenile LPP, FFA and DLE exist but are rare; management mirrors adults, with extra caution for steroid atrophy and the growth effects of systemic agents.[1]

African ancestry and CCCA

A woman of African ancestry with vertex hair loss has CCCA until proven otherwise. Take a sensitive hair-care history — patients may not see tight braids, weaves or relaxers as harmful. Counselling on protective styling (low tension, no chemicals, no heat) is as important as any drug. AKN in Black men needs the same culturally sensitive advice on clipping and friction.[1]

Elderly patients

Postmenopausal frontal recession is the FFA signature. But elderly scalp brings atrophy, actinic damage and comorbidity that magnify steroid and immunosuppressant risk. Hydroxychloroquine retinopathy climbs with age and duration — ophthalmology screening matters most here.[1]

Immunocompromised patients

In HIV, transplant or other immunosuppression, think infection and malignancy first: disseminated tinea, deep fungal infection, cutaneous TB and lymphoma can all scar. Biopsy and culture before any immunosuppression.[1]

Evidence, guidelines and regional deltas

The NAHRS classification — first published in 2001 and refined at later consensus meetings — is still the international scaffold. It is purely descriptive, sorting disease by infiltrate, but it earns its keep by giving treatment a rational base.[6]

High-quality randomised trials are scarce because the diseases are rare and heterogeneous, so most evidence is case series, expert consensus and retrospective cohorts. The anchors worth naming:[1]

• Hydroxychloroquine is the commonest systemic agent for lymphocytic disease, backed by retrospective series and consensus; allow a 6-month trial before calling failure.
• Rifampicin-clindamycin is the accepted regimen for folliculitis decalvans, supported by small cohorts and the biofilm-eradication rationale.
• Isotretinoin is the mainstay for dissecting cellulitis, on case series and expert recommendation.
• TNF inhibitors (adalimumab, infliximab) have emerging evidence in refractory neutrophilic and mixed disease, including dissecting cellulitis and AKN.
• JAK inhibitors are increasingly reported for refractory LPP and FFA, but long-term safety is thin and use is off-label.

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Regional differences are real. In India and many low-resource settings, hydroxychloroquine is affordable and available, but isotretinoin needs a strict pregnancy-prevention programme and rifampicin-clindamycin may be limited by cost or access. In the UK, NICE and British Association of Dermatologists guidance stress photoprotection in DLE and shared-care biologics prescribing. In the US, American Academy of Dermatology consensus backs mechanism-based therapy and early biopsy. In Europe, EADV consensus foregrounds psychosocial impact and quality-of-life assessment. Follow local formularies and pregnancy-prevention rules.[3]

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Exam pearls — what the viva is really asking

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The mantra

Lost ostia are lost forever — treat the margin, not the scar. Biopsy the active border, name the infiltrate, douse the inflammation early, and never promise regrowth from skin that has already turned to collagen.[1][10]

Ward-round test — three stems

Stem 1 — the postmenopausal hairline (answer)

The 64-year-old woman from the top of the topic. The dermatoscope shows no follicular ostia over the receded frontal band, a single terminal hair at the leading edge, and perifollicular erythema and scale. Her eyebrows are thin. What is the diagnosis, the first investigation, and the first treatment step? Model: This is frontal fibrosing alopecia (FFA), a lymphocytic cicatricial alopecia — the lonely hair sign plus frontal-temporal recession in a postmenopausal woman with eyebrow loss is near-pathognomonic. Confirm with a 4 mm punch biopsy of the active inflammatory margin (not the smooth scarred centre). Start potent topical corticosteroid to the active margin plus intralesional triamcinolone, and begin hydroxychloroquine (under 5 mg per kg per day, with baseline ophthalmology). Counsel honestly: treatment halts progression but cannot regrow the scarred band. Strict sun protection and a 5-alpha-reductase inhibitor are commonly added.[1][6]

Stem 2 — the young man with the boggy scalp (answer)

A 26-year-old Black man presents with deep, tender, boggy nodules and abscesses across his scalp, connected by sinus tracts discharging pus. He also has severe nodulocystic acne and axillary hidradenitis suppurativa. What syndrome, what first-line drug, and what long-term danger must you name? Model: This is dissecting cellulitis of the scalp, one limb of the follicular occlusion tetrad (with acne conglobata, hidradenitis suppurativa and pilonidal sinus). First-line is oral isotretinoin 0.5 to 1 mg per kg per day for 4 to 6 months, with strict pregnancy prevention. TNF inhibitors (adalimumab, infliximab) are reserved for refractory disease, and surgery only in quiescent, localised disease — operating on active inflammation flares it. The long-term danger is squamous cell carcinoma (Marjolin ulcer) in a chronic non-healing sinus: biopsy any ulcer that will not close.[3][7]

Stem 3 — the child sent as 'alopecia areata' (answer)

A 7-year-old has a boggy, tender, purulent, balding plaque on the scalp with occipital lymphadenopathy. The registrar wants to start intralesional triamcinolone for presumed alopecia areata. What is the likely diagnosis, and what is the right treatment? Model: This is a kerion — an inflammatory dermatophyte (tinea capitis) infection, not alopecia areata. The boggy purulent plaque plus occipital lymphadenopathy in a child is the classic picture, and untreated it scars. The right move is oral antifungal therapy — griseofulvin or terbinafine for 6 to 8 weeks — not corticosteroid, which would worsen a dermatophyte infection. Confirm with KOH microscopy and fungal culture of skin scrapings and hairs. The trap to name: immunosuppressing a kerion is the recurring error that converts a curable infection into permanent scarring alopecia.[1][6]

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References

1. [1]Griggs J, Trüeb RM, Gavazzoni Dias MFR, et al. Fibrosing alopecia in a pattern distribution J Am Acad Dermatol, 2021.PMID 31926219
2. [2]Pirmez R. The dermatoscope in the hair clinic: Trichoscopy of scarring and nonscarring alopecia J Am Acad Dermatol, 2023.PMID 37591567
3. [3]Ezemma O, Devjani S, Kelley KJ, et al. Treatment modalities for lymphocytic and neutrophilic scarring alopecia J Am Acad Dermatol, 2023.PMID 37591564
4. [4]Mathur M, Acharya P Trichoscopy of primary cicatricial alopecias: an updated review J Eur Acad Dermatol Venereol, 2020.PMID 31566830
5. [5]Harries M, Imanishi H, Paus R Fibrosis and stem cell epithelial-mesenchymal transition in primary cicatricial alopecias J Am Acad Dermatol, 2019.PMID 30639879
6. [6]Uchiyama M Primary cicatricial alopecia: Recent advances in evaluation and diagnosis based on trichoscopic and histopathological observation, including overlapping and specific features J Dermatol, 2022.PMID 34866229
7. [7]Sood S, Sriranganathan A, Heung M, et al. Biologic and Small Molecule Treatments for Primary Neutrophilic Cicatricial Alopecias: An Evidence-Based Review J Cutan Med Surg, 2023.PMID 37489902
8. [8]Wang EHC, Monga I, Sallee BN, et al. Primary cicatricial alopecias are characterized by dysregulation of shared gene expression pathways PNAS Nexus, 2022.PMID 35899069
9. [9]Heymann WR. Central centrifugal cicatricial alopecia: Beyond the hot comb J Am Acad Dermatol, 2023.PMID 37775048
10. [10]Jimenez F, Alam M, Vogel JE, et al. Hair transplantation: Basic overview J Am Acad Dermatol, 2021.PMID 33905785